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11
Effects of Exposure to Environmental Tobacco Smoke on Lung Function and Respiratory Symptoms

This chapter discusses epidemiologic studies of nonsmokers exposed to tobacco product smoke that have evaluated lung function or respiratory symptoms, most of which have evaluated children. The effects of active cigarette smoking are briefly reviewed to recount the reasons why certain aspects of lung function have been studied in nonsmokers. The plausibility of finding similar effects in nonsmokers exposed to ETS is discussed and the studies found in the literature are assessed.

LUNG FUNCTION AND SYMPTOMS IN ACTIVE SMOKERS

Cross-sectional studies of smokers have demonstrated that smokers, compared with nonsmokers, have (1) an increased prevalence of chronic cough, chronic sputum production, and wheezing and (2) decreased lung function (see U.S. Public Health Service, 1984, for an extensive review). The effects of smoking on both respiratory symptoms and lung function may be seen within a few years of the onset of regular smoking (U.S. Public Health Service, 1979, 1984; Woolcock et al., 1984). Longitudinal studies have demonstrated that the mean rate of decline with age of the 1-second forced expiratory volume (FEV1) is greater in smokers than in nonsmokers. In some smokers, the rate of decline of FEV1 is rapid, leading to clinically important chronic airflow obstruction.

The structural changes associated with active cigarette smoking are seen in both the conducting airways and the pulmonary parenchyma (for a more detailed description, see U.S. Public



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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects 11 Effects of Exposure to Environmental Tobacco Smoke on Lung Function and Respiratory Symptoms This chapter discusses epidemiologic studies of nonsmokers exposed to tobacco product smoke that have evaluated lung function or respiratory symptoms, most of which have evaluated children. The effects of active cigarette smoking are briefly reviewed to recount the reasons why certain aspects of lung function have been studied in nonsmokers. The plausibility of finding similar effects in nonsmokers exposed to ETS is discussed and the studies found in the literature are assessed. LUNG FUNCTION AND SYMPTOMS IN ACTIVE SMOKERS Cross-sectional studies of smokers have demonstrated that smokers, compared with nonsmokers, have (1) an increased prevalence of chronic cough, chronic sputum production, and wheezing and (2) decreased lung function (see U.S. Public Health Service, 1984, for an extensive review). The effects of smoking on both respiratory symptoms and lung function may be seen within a few years of the onset of regular smoking (U.S. Public Health Service, 1979, 1984; Woolcock et al., 1984). Longitudinal studies have demonstrated that the mean rate of decline with age of the 1-second forced expiratory volume (FEV1) is greater in smokers than in nonsmokers. In some smokers, the rate of decline of FEV1 is rapid, leading to clinically important chronic airflow obstruction. The structural changes associated with active cigarette smoking are seen in both the conducting airways and the pulmonary parenchyma (for a more detailed description, see U.S. Public

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects FIGURE 11–1 Known and suspected mechanisms for effects of tobacco smoke on airways. Solid lines=known mechanisms; dashed lines=suspected mechanisms. Health Service, 1984). In the large airways there is hypertrophy and hyperplasia of the mucous glands. These changes are followed by an increase in mucus production that leads to increased cough and sputum production. Structural changes in smaller airways range from relatively mild inflammation to narrowing and closure of airways due to inflammation, goblet cell hyperplasia, and intraluminal mucus. Changes in the parenchyma include increased numbers of inflammatory cells and ultimately destruction of the alveolar walls, most commonly in the central part of the lobule, i.e., the development of centrilobular emphysema (see Figure 11–1). The link between airway disease and parenchymal disease is poorly understood. Smokers with severe functional impairment usually have an appreciable amount of emphysema (U.S. Public Health Service, 1984). Cessation of smoking leads to a rapid decrease in respiratory symptoms, an improvement in lung function, and a shift towards the nonsmoker’s rate of decline of FEV1 (U.S. Public Health Service, 1979, 1984). These improvements are usually seen regardless of the functional level at which cessation occurs.

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects Population-based studies of adults have generally shown a strong dose-response relationship between FEV1 with dose measured either in terms of years smoked, the number of cigarettes per day, or the integrated dose, i.e., pack-years (U.S. Public Health Service, 1984). It is worthwhile noting, however, that in two major studies (Burrows et al., 1977a; Beck et al., 1981) the active smoking dose accounted for only about 15% of the variation of FEV1 even after age and height adjustment. Most of the variance could be attributed to the naturally occurring large variability in pulmonary function. Another reason the active smoking dose did not explain much of the variance is that the number of cigarettes an individual smokes cannot readily be translated into the dose of smoke that is delivered into the airways and parenchyma. Many factors, such as puff volume and lung volume at which inhalation starts, clearance rates, and airway geometry of the lungs of exposed individuals, will influence the dose and the distribution of the smoke within the lungs. Variability in individual susceptibility to the effects of chemicals deposited in the lung has been demonstrated in studies of animals (Evans et al. 1971, 1975, 1978). PLAUSIBILITY FOR AN EFFECT DUE TO PASSIVE SMOKING The dose of cigarette smoke delivered to the lungs of nonsmokers exposed to ETS is both qualitatively and quantitatively different from mainstream smoke, being a small fraction of that delivered to the lungs of an active smoker (see discussions in Chapter 7). Exposure to constituents of tobacco smoke may begin in utero and continue throughout childhood through ETS exposure. During these periods, the lung is undergoing both growth and remodeling. Therefore, the lung of the fetus and young child may be particularly susceptible to environmental insults. Despite qualitative differences between mainstream smoke, sidestream smoke, and ETS, it has been customary to assume that exposure to ETS approximates a low-dose exposure to tobacco smoke. The ability to measure responses to low doses depends on the shape of the dose-response curves, the sensitivity and specificity of the measurement tools available, and whether there is a threshold of exposure below which there is no response in any individual.

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects The assumed shape of the dose-response curve determines what kinds of effects would be expected and the estimates of the probability of detecting them. If the dose-response curve were linear with a shallow slope, or a slope concave to the dose axis, the response at low doses might be so small that it would be difficult to detect. In such a situation, only the very susceptible portion of the population might have detectable effects. It is likely that there is a distribution of susceptibility to the effects of ETS within the population, such that there will be some persons who will respond at low doses and some persons for whom many years of heavy exposure may be needed to cause the same symptoms or change in lung function (Cockcroft et al., 1983). If individuals who are most susceptible to the irritating effects of cigarette smoke on the lower respiratory tract do not start to smoke or, having started, soon quit as smokers, then a population of nonsmokers would be more likely to include the most susceptible individuals than a population of smokers. The existence of different subpopulations introduces an additional complication to the extrapolation from high-dose exposure in active smokers to the low-dose exposures of nonsmokers. In addition, it is likely that the development of respiratory disease or symptoms, lung function level, and rate of decline reflect the cumulative burden of many environmental exposures and other insults, such as respiratory infections (Purvis and Ehrlich, 1963) to the lung. Furthermore, it might be hypothesized that the cumulative burden may interact with the individual’s genetically determined susceptibility. METHODOLOGIC CONSIDERATIONS FOR EPIDEMIOLOGIC STUDIES A recent report of the National Research Council (1985) is devoted to methodologic issues of epidemiology and air pollution. In this section, many of the problems are reviewed briefly. Study Design and Analysis Chronic pulmonary effects of ETS have been the subject of several recent reviews (Lee, 1982; Weiss et al., 1983; Surgeon General, 1984; Guyatt and Newhouse, 1985; Taylor et al., 1985) and symposium or workshop reports (U.S. Public Health Service,

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects 1983; Gammage and Kaye, 1984; Rylander, 1984). Many of the studies reported in these reviews had not been originally designed to study chronic pulmonary effects of ETS exposure. Instead, these data sets were reanalyzed to address the question of the pulmonary effects of ETS. This use of these studies suggests the need for caution when interpreting their results. Several analytic approaches were used in the reported studies. Independent risk factors, such as age and sex, usually need to be taken into account, but this was not always done. Several statistical approaches, such as stratification or regression analysis, are used to take into account the effects of potentially confounding variables. For most of the potentially confounding variables, researchers do not agree on the nature of the roles of the variables as confounders and, hence, on the appropriate ways to introduce these variables into the data analyses. Assessing Exposure Interpretation of epidemiological studies is hampered by the existence of factors that interact with and modify the response to exposure and by confounding factors that are associated with the same symptom complex as exposure to ETS, such as coughing, production of sputum, and wheezing (see Table 11–1). These variables must be assessed and accounted for in the statistical analyses where possible. Unreported active smoking could lead to a large bias. Underreporting of smoking is likely in studies of older children, particularly when parents answer questionnaires for their children. Children who have parents who smoke are themselves more likely to smoke. Therefore, because active smoking is likely to have a considerably greater impact on respiratory symptoms and lung function than exposure to ETS, misclassification of the children who smoke will tend to overestimate the effect of exposure to ETS. For blue collar males, occupational exposure can also be important and may interact with both direct cigarette smoke and ETS. Many pulmonary toxicants can exist in the workplace. Furthermore, ETS exposure can occur in the workplace. Similarly, comparison of inner-city-dwelling persons with less urban, or sub-urban, controls can lead to biases.

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects TABLE 11–1 Potentially Confounding and Effect Modifying Factors in Epidemiologic Studies of Exposure to Environmental Tobacco Smoke Unreported active smoking Tobacco products Marijuana Clove cigarettes Developmental factors Maternal smoking during pregnancy Factors related to outdoor environment Outdoor temperature, humidity Respirable and nonrespirable particulates, e.g., fugitive dust Pollens and other allergens Factors related to indoor environment Crowding Number and age of siblings Total number of people/animals in dwelling unit Total number of smokers in dwelling unit Household conditions Frequency of air exchanges Temperature and humidity Use and condition of air conditioning units Conditions of child care facilities Unvented combustion products from heating/cooking stoves Respirable and nonrespirable particulates, e.g., wood smokes Pollens, molds, mites Allergens and infectious organisms Formaldehyde Factors related to work/hobbies Work/hobby-related exposure to gases, fumes, particulates Miscellaneous factors Annoyance response to tobacco smoking Reporting biases Assessing Respiratory Variables Methods commonly used to assess the effect of passive smoking on the respiratory system, such as respiratory symptom questionnaires and measurement of lung function, may lead to some error. The problems associated with the respiratory symptom questionnaires include: Different questionnaires are used in studies. Differences in how the questions are asked can sometimes lead to large differences in answers. For instance, asking “Are you a smoker?” may elicit a “No” response from an exsmoker whereas the question “Have you ever smoked?” would be answered “Yes”.

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects Some studies use a self-administered questionnaire, whereas other studies use a trained interviewer. Trained interviewers can determine whether the subject understands the questionnaire and can follow a prescribed set of probing questions that may help to resolve the specific nature of not-well-described symptoms. Some studies have parents complete the questionnaires for the children, whereas other studies have the child answer the questionnaire. For older children, parents may not be aware of active smoking by the child and exposures to ETS in environments outside the home. Questionnaires necessarily involve some subjective elements that are prone to recall bias. For example, a smoker who is symptomatic may be more likely to report the same symptom in his/her child (Schenker et al., 1983; Ferris et al., 1985). Many tests are prone to measurement error, which tends to obscure differences between groups of subjects. For example, it may be necessary to repeat lung function measurements for a given individual and to average results to get a reliable estimate. Lung function tests are often not sensitive to the structural and functional changes associated with lung disease (Drill and Thomas, 1980). CROSS-SECTIONAL STUDIES In the following sections, selected cross-sectional studies of respiratory symptoms, lung function, and respiratory infections and longitudinal studies of lung functions are reviewed. The studies reviewed here are larger studies in which attempts have been made to standardize assessments and many of the data-gathering techniques, including interviews. Studies of Respiratory Symptoms in Children Almost all of the cross-sectional studies that have compared children of parents who smoke with the children of parents who do not smoke have reported increased prevalences of respiratory symptoms, usually cough, sputum, or wheezing, in the children of smoking parents. Some studies, including some that have not found a statistically significant increase in the prevalence of respiratory symptoms in ETS exposed children, have demonstrated

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects an increase in respiratory symptom prevalence with an increasing number of parents or other adults who smoke in the home (see below). Three problems are especially important for studies of respiratory symptoms in children, i.e., underreported active smoking on the part of children, recall bias leading to overreporting of symptoms by parents, and the confounding variables of infections in parents. All three may lead to overestimation of symptom prevalences among children of smokers. Recall bias would occur if parents who have respiratory symptoms are more likely to report those symptoms in the children. (The possiblity also exists that parents with these symptoms would look upon them as so commonplace as not to be worthy of mention). Parents who are smokers are also more likely to have more respiratory symptoms and respiratory infections. Respiratory infections (and, as a consequence, symptoms) among children of smokers may be the result of direct transmission of infectious agents from the parent or may be caused by inflammation and irritation of lung tissues due to ETS exposure and consequent increase in susceptibility to infection. It has been observed that parents, especially mothers, who have a history of severe respiratory illness report higher rates of respiratory symptoms in their children (Schenker et al., 1983; Ferris et al., 1985). Various ways of dealing with these potential sources of bias have been proposed. Restricting the study or analysis to children below age 8 is likely to eliminate bias due to underreporting of children who currently smoke. It is more difficult to handle the overreporting of symptoms in children when the parents have respiratory symptoms. An additional problem for interpretation of parental reports of respiratory symptoms was noted by Schenker et al. (1983). In their study, children whose questionnaires were completed by fathers had significantly fewer symptoms reported than children with mother-completed questionnaires. There was no comparison of questionnaires completed separately by both mother and father for the same child. Because the rates for symptoms as reported by the mother were similar to what was found in other studies and because the fathers reported significantly fewer symptoms, the investigators suggested that fathers underreported symptoms in their children.

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects Table 11–2 reviews several selected cross-sectional studies of respiratory symptoms in children and adults. Lebowitz and Burrows (1976), reporting on children in the Tucson Epidemiologic Study of Obstructive Lung Disease, emphasized the need for controlling for parental symptoms. They reported that children had a higher prevalence of respiratory symptoms if they lived in households with adults with the same symptom, regardless of the family smoking habits. When the presence of symptoms in the adults was taken into account by partitioning households based on presence or absence of adult symptoms(s), the odds ratio that remained was greater than unity but was no longer statistically significant [Mantel-Haenszel odds ratio for all respiratory symptoms calculated from data presented is 1.35 (95% confidence limits of 0.91 to 1.98)]. Most symptoms were reported more frequently for children in currently smoking families. Ferris et al. (1985) have argued that correcting for parental symptoms represents an overcorrection for respiratory symptoms in children since it also corrects for the parents’ smoking habits. In the Harvard Air Pollution Respiratory Health Studies (Six-Cities Study) of 10,106 white children aged 6–9 years, the variable indicating whether the parent had a history of bronchitis, emphysema, or asthma was found to be a highly significant independent risk factor for cough and wheeze and a history of respiratory illness among children (Figure 11–2). Children whose parents had a positive history had 72–155% higher symptom and illness rates than children whose parents had no history of these illnesses. Adjustment for parental respiratory history reduced the size of the estimated effects of maternal smoking on respiratory symptoms and illnesses by 20 to 30%, but the associations remained statistically significant for most of the outcome symptom and respiratory illness variables (odds ratios of 1.23 and 1.28, respectively). In both the Lebowitz and Ferris studies, adjustment for parental symptoms or respiratory illness decreased the strength of the apparent association between exposure to ETS and respiratory symptoms, but did not eliminate it. This finding leads to the reasonable conclusion that the exposures typical of ETS are sufficient to cause respiratory symptoms in some children. The increases in frequency of cough were 20 to 50%, and as high as 90%, when there were smoking parents. The increases in frequency of wheezing were more variable, which may indicate the difficulty in

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects TABLE 11–2 Effects of Passive Smoking on Respiratory Symptoms: Selected Cross-sectional Studies Involving Children/Adolescents Study Source of Subjects Subjects Exposure Assessment Findings Comments Colley, 1974 Aylesbury, UK; seven public schools; 1971 1,328 boys, 270 girls; ages 6–14 Self-administered questionnaire from parents Close association of child cough and parent winter morning phlegm Prevalence of cough, 15.6% no smokers, 22.2% both parents smoke (ns) Suggested cross-infection may be important cause; used different question from U.S. studies Lebowitz and Burrows, 1976 Tucson, Ariz.; stratified cluster random sample of households; 1972–1973 1,655 households; Anglo-white; 1,252 children <16, 2,516 children >15 Self-administered NHLBI questionnaire from children >15; otherwise from parents Prevalence of cough in young children, 7.8% no smokers, 10.4% smokers (p<0.05) Significance gone when parental symptoms considered Less than 15 years old assumed to be nonsmokers; concluded familial aggregation important, potential confounder Schilling et al., 1977 Survey of towns in Connecticut and South Carolina 816 children in 376 families; 607 children <16, 109 children >15 Respiratory Symptom Questionnaire, administered by interviewer No effect of parental smoking on children’s cough or wheeze Prevalence of wheeze in young children related to parental wheeze (p<0.01) Tried to account for active smoking in children Bland et al., 1958 Derbyshire, UK; 48 secondary schools; 1974 2,847 boys, 2,988 girls; 12 years old Self-administered questionnaire by child Prevalence of cough, 16% no smokers, 19% one smoker, 23.5% two smokers (p<0.01) Effects of child’s and parent’s smoking independently analyzed.

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects Study Source of Subjects Subjects Exposure Assessment Findings Comments Tager et al., 1979 East Boston, Mass.; random sample in schools; 1975–1977 444 children; ages 5–9 years NHLBI questionnaire administered by interviewer; if age <10, parent answered No increase in respiratory illness with parental smoking Controlled for family size Weiss et al., 1980 See Tager et al., 1979 650 children; ages 5–9 years See Tager et al., 1979 Persistent wheeze, 1% no smokers, 6.8% one smoker, 11.8% two smokers (p<0.02) See Tager et al., 1979 Dodge, 1982 Three towns in Arizona; survey of schools; 1978–1979 558 children; ages 8–10 years Self-administered by parents Child’s wheeze (p<0.05), sputum (p<0.05), and cough (p<0.01) related to parental smoking   Schenker et al., 1983 Pennsylvania; survey of schools 4,071 children; ages 5–14 Self-administered by parents Trend with number of smoking parents not significant for any symptoms Not adjusted for parental symptoms although found to influence no. symptoms reported Ware et al., 1984 Six U.S. cities; different regions survey of schools; 1974–1979 10,106 children; ages 6–13 Self-administered by parents 20–35% increased risk of all respiratory illness and symptoms with maternal smoking Multiple logistic regression with gas cooking as other predictor

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects carryover effect into later childhood and adult life. Direct effects of ETS as an airway irritant are also likely, although the dose by itself may be insufficient except for the most susceptible individuals to cause symptoms and/or functional impairment. It is unlikely that exposure to ETS can cause much emphysema. As one of the many pulmonary insults, however, ETS may add to the total burden of environmental factors that become sufficient to cause chronic airway or parenchymal disease. STUDIES OF ACUTE PULMONARY EFFECTS Several studies have examined acute responses to ETS. Because asthmatics may be hypersensitive to exposures to noxious agents, a number of studies have also searched for acute effects of exposure to ETS among asthmatic populations. Other studies have been conducted on normal healthy adults. Normal Subjects Pimm et al. (1978) compared various physiologic responses of nonsmokers to either room air or room air plus machine-generated cigarette smoke. Each smoke exposure consisted of combustion of four cigarettes to produce an extremely polluted room with high levels of carbon monoxide (24 ppm) and particles (greater than 4 mg/m3). Pulmonary function tests, nitrogen washout curves, blood carboxyhemoglobin levels, and heart rates were measured before, during, and after a 2-hour exposure. A few statistically significant differences between smoke and ambient air exposure days were found. The differences were small and were considered by the investigators to be of questionable importance. Subjective complaints were common in this and other acute cigarette smoke exposure studies, particularly eye irritation and cough. CO and suspended particles are thought to be less important than the phenols, aldehydes, and organic acids in producing this symptomatology (Hinds and First, 1975). Shephard et al., (1979b) utilized a protocol similar to Pimm et al. (1978) but under conditions of intermittent moderate exercise (increasing the respiratory volume per minute 2.5 times). Moderate and heavy ETS exposures were considered, associated with CO concentrations of 20 and 31 ppm, respectively. Neither exercise

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects TABLE 11–8 Pneumonia and Bronchitis by Parents Smoking in First Year of Follow-up, Annual Incidence per 100 Children (Number of Infants in Parentheses) Both Nonsmokers Both or One Exsmokers or Smoking Habits Changed One Smoker Both Smokers All 7.8 (372) 9.2 (675) 11.4 (552) 17.6 (478) 11.5 (2,077)   SOURCE: Colley et al. (1974). nor exposure level significantly influenced symptomatology. Small decrements (3–4%) in FVC, FEV1, Vmax50%, and Vmax25% (the volumes of air expired during the first half of the period of forced expiration or first quarter of the period, respectively) were noted in response to smoke exposures; however, static lung volumes were unaffected. Eye irritation and odor complaints were very common. One subject complained of wheezing and chest tightness, although his pulmonary function was not significantly impaired. Subjective symptom scores were higher overall for the higher smoke exposure (13.8 versus 10.3 points/subject at the lower exposure). A few subjects reported cough, nasal discharge, or stuffiness and throat irritation. Asthmatic Subjects A number of studies have examined acute pulmonary responses of asthmatic patients to exposure to ETS (Table 11–8). However, the mechanisms for bronchoconstriction among asthmatics differ. Therefore, the comparison between study populations and between individuals within studies is difficult. Shephard et al. (1979a) examined asthmatic persons to determine whether their response to ETS exceeded that of normal subjects in a previous study. The subjects (9 men and 5 women; average age, 37 years) were exposed for 2 hours to machine-generated smoke (CO, 24 ppm). None of the patients had current respiratory infections, but some may have had associated chronic bronchitis or pulmonary emphysema. No significant alterations in dynamic lung volumes (FEV1, Vmax50%, and Vmax25%) were detected when the asthmatics’ responses to ambient air and cigarette smoke were

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects compared. A small, but significant, decrease in total lung capacity (TLC) was noted, although preexposure TLC was slightly higher than that on the same exposure day (96.5% and 103.5% relative to ambient air TLC, respectively). The lack of measurable change was interesting in light of a reported history of exacerbation with exposure to ETS by four subjects. Acute symptomatic responses during the experimental study were similar to those seen in the investigators’ previous study of normal individuals; however, more complaints of tightness in the chest (43% of subjects) and wheezing (36%) were made by asthmatic subjects. It was concluded that asthmatics did not have unusual measurable responsiveness to ETS exposure in this study. The findings of Dahms et al. (1981) contrast with those of Shephard et al. (1979a). The exposure in this study was less intense, i.e., 1 hour at CO levels of 15–20 ppm. The patients were 16 to 39 years old, had mild impairment, and were on medication, except for the restriction that no bronchodilators might be used within 4 hours previous to the test. Five of the patients reported specific complaints when exposed to ETS. When compared with control subjects, asthmatics showed significant pulmonary function changes following 1 hour of smoke exposure. FVC decreased 20% and FEV1 declined 21.4% in the asthmatic subjects. These decreases are very large compared with the other studies. Based on a 0.40% increase in blood carboxyhemoglobin, the environmental CO concentration was calculated to be between 15 and 20 ppm—compared with approximately 24 ppm in the Shephard et al. (1979a) studies. Reasons for the discrepancy between the Dahms and Shephard studies results are not clear, nor do Dahms et al. (1981) cite or discuss the earlier Shephard et al. (1979a) findings. Knight and Breslin (1985) evaluated six nonsmoking patients. The details of the subject population and exposure conditions were not specified. They measured a mean fall in FEV1 of 11% following exposure to ETS. Using a histamine inhalation test, they found that the provocative concentration (or dose) that produced a 20% fall in FEV1 (PC20FEV1 or PD20FEV1) decreased following exposure to ETS. This indicates an increased bronchial reactivity to histamine. The authors hypothesized that the airways may be primed to react more vigorously to other triggers. Wiedemann et al. (1986) evaluated nine asthmatic individuals (aged 19 to 30 years) with normal or nearly normal lung function

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects for both lung function and airway reactivity following exposure to ETS. Six patients reported a history of reaction to ETS. These subjects, all of whom were off medication, were exposed for 1 hour (CO between 40 and 50 ppm). Their carboxyhemoglobin levels increased an average of 0.86% (p<0.001), FVC decreased 2% (p<0.01), and FEV1 declined 1% (not statistically significant). Airway reactivity was assessed using a methylcholine challenge test. The PD20FEV1 increased from 0.25±0.22 on the day before exposure to 0.79±1.13 postexposure (p<0.05), indicating a decrease in airway reactivity following exposure. The magnitude of this decrease was small, and the clinical meaning of the change is uncertain. There are a number of possible reasons for the apparent inconsistency among these studies, not the least of which is small sample sizes. The subjects have not been characterized fully. As noted by the authors, the stability of patients and mechanisms of bronchoconstriction differ among subjects. For instance, patients were included in several of these studies, regardless of whether they were hypersensitive on the methylcholine challenge test. Further, some studies were performed on medicated patients. None of the studies could be performed blind to the presence of ETS. Therefore, the authors could not exclude the possibility that pulmonary function changes could be emotionally related to cigarette smoke exposure, especially in those patients who reported previous histories of adverse response to ETS exposure. There are several issues that are unresolved by these studies. For instance, what proportion of a clearly defined population of asthmatics do react to ETS? If the patients are selected according to methylcholine or histamine responsiveness, criteria should be given for the extent of responsiveness, since it is a continuum. To address the issue of degrees of sensitivity, the appropriate case-control or cross-over studies, with carefully selected populations, need to be done. Mechanisms of Response The mechanisms responsible for eye irritation and rhinitis, as well as possible changes in airway size, are almost entirely unknown. They could represent irritant effects from gases such as oxides of nitrogen, acrolein, ammonia, and other reactive constituents. Lundberg et al. (1983) reported that throat irritation

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects and local edema may be due to vapor-phase components that stimulate substance P release from local capsaicin-sensitive afferent neurons in the airway mucosa. It is also possible that an allergic mechanism could be involved. Several authors have described allergic reactions to cigarette smoke (see, for example, Zussmann, 1970). Cutaneous hypersensitivity to tobacco antigens has been described in clinical settings (Becker et al., 1976). Constituents of tobacco smoke have also been shown to be immunogenic in laboratory animals (Becker et al., 1979; Gleich and Welsh, 1979). During the last 10 years, Becker and colleagues (1979, 1981; Becker and Dubin, 1977) have isolated a tobacco glycoprotein both from cured tobacco leaves as well as from cigarette smoke condensate. Animals that were previously sensitized to this antigen had both pulmonary and cardiovascular changes when challenged (Levi et al., 1982). However, the role, if any, of this antigen, as well as other antigens that may be present in tobacco smoke, in the pathogenesis of cardiopulmonary disease in active smokers, let alone nonsmokers exposed to ETS, remains controversial. SUMMARY AND RECOMMENDATIONS There have been many studies of respiratory effects of exposure to ETS to children. In view of the weight of the scientific evidence that ETS exposure in children increases the frequency of pulmonary symptoms and respiratory infection, it is prudent to eliminate smoking and resultant ETS from the environments of small children. What Is Known Children of parents who smoke compared with the children of parents who do not smoke show increased prevalences of respiratory symptoms, usually cough, sputum, and wheezing. The odds ratios from the larger studies, adjusted for the presence of parental symptoms, were 1.2 to 1.8, depending on the symptoms. These findings imply that ETS exposures cause respiratory symptoms in some children. Estimates of the magnitude of the effect of parental smoking on FEV1 function of children range from zero to approximately 0.5% decrease per year. This small effect is unlikely by itself to be clinically significant. However, it may reflect pathophysiologic

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects effects of exposure to ETS in the lungs of the growing child and, as such, may be a factor in the development of chronic airflow obstruction in later life. Bronchitis, pneumonia, and other lower-respiratory-tract illnesses occur up to twice as often during the first year of life in children who have one or more parents who smoke than in children of nonsmokers. What Scientific Information Is Missing ETS exposure during childhood may influence the development of airway hyperresponsiveness in adult life. Research is needed to address this issue. To evaluate the timing of physiologic changes during development may require animal studies. Future cross-sectional studies of ETS exposure and lung function in adults need to be designed to control for other factors that may affect lung function. Little information is available from long-term longitudinal studies of the effect of exposure to ETS by nonsmokers on lung function in either children or adults. Studies need to be carried out in areas with different climates and characteristics of housing over long enough periods of time to assess the effects of changing smoking patterns. Animal studies may also be required to address these longitudinal questions. Intervention studies, in which parents stop smoking in the presence of children, should be done to assess the reversibility of these effects. The pathophysiologic mechanism of increased susceptibility to viral infections in very young children exposed to ETS has not been clarified. The extent to which normal and asthmatic adults are affected by short-term exposures to ETS needs to be studied further. The few studies of the effect of short-term ETS exposure of asthmatic patients and of nonasthmatics are not consistent. This may be because they have not been conducted under adequate control and have examined persons with considerable variability in the severity of asthmatic disease and airway responsiveness. Future studies should carefully define the populations when addressing issues of frequency of reaction to ETS and should be done separately on hyperresponsive and nonhyperresponsive patients when addressing issues of severity of reaction to ETS.

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects Studies of other patients with obstructive lung disorders, such as cystic fibrotic and alpha-1-antitrypsin patients, need to be done. Future studies need to identify susceptible subpopulations, if they exist, who are unusually vulnerable to the acute effects of ETS exposure. There is no consensus on how to deal with data on parental respiratory symptoms. Investigations should report on rates of childhood illness/symptoms using analyses that are both adjusted and unadjusted for parental symptoms. There is need for information on changes in pulmonary function between the end of the peak growth period and adult life to assess the possible reversibility of effects. REFERENCES Adlkofer, F., G.Scherer, and H.Weimann. Small-airways dysfunction in passive smokers. N. Engl. J. Med. 303:392, 1980. Aviado, D.M. Small-airway dysfunction in passive smokers. N. Engl. J. Med. 303:393, 1980. Beck, G.J., C.A.Doyle, and E.N.Schachter. Smoking and lung function. Am. Rev. Respir. Dis. 123:149–155, 1981. Becker, C.G., T.Dubin, and H.P.Wiedemann. Hypersensitivity to tobacco antigen. Proc. Natl. Acad. Sci. USA 73:1712–1716, 1976. Becker, C.G., and T.Dubin. Activation of factor XII by tobacco glycoprotein. J. Exp. Med. 146:457–467, 1977. Becker, C.G., R.Levy, and J.Zavecz. Induction of IgE antibodies to antigen isolated from tobacco leaves and from cigarette smoke condensate. Am. J. Pathol. 96:249–254, 1979. Becker, C.G., N.Van Hamont, and M.Wagner. Tobacco, cocoa, coffee, and ragweed: Cross-reacting allergens that activate factor-XII-dependent pathways. Blood 58:861–867, 1981. Berkey, C.S., J.H.Ware, D.W.Dockery, B.G.Ferris, Jr., F.E.Speiger. Indoor air pollution and pulmonary function growth in preadolescent children. Am. J. Epidemiol. 123:250–260, 1986. Bland, M., B.R.Bewley, V.Pollard, and M.H.Banks. Effect of children’s and parents’ smoking on respiratory symptoms. Arch. Dis. Child. 53:100–105, 1978. Brunekreef, B., P.Fischer, B.Remijn, R.Van der Lende, J.Schouten and P.Quanjer. Indoor air pollution and its effect on pulmonary function of adult non-smoking women. III. Passive smoking and pulmonary function. Int. J. Epidemiol. 14:227–230, 1985. Burchfiel, C.M., M.W.Higgins, J.B.Keller, W.J.Butler, W.F.Howatt, and I.T.T.Higgins. Passive smoking, respiratory symptoms and pulmonary function: A longitudinal study in children. Am. Rev. Respir. Dis. 133:A157, 1986.

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